Relevant bibliographies by topics / H-RasV12

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Academic literature on the topic 'H-RasV12'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "H-RasV12"

1

Telang, Sucheta, Andrew N. Lane, Kristin K. Nelson, Sengodagounder Arumugam, and Jason Chesney. "The oncoprotein H-RasV12 increases mitochondrial metabolism." Molecular Cancer 6, no. 1 (2007): 77. http://dx.doi.org/10.1186/1476-4598-6-77.

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2

Sagini, Krizia, Lorena Urbanelli, Eva Costanzi, et al. "Oncogenic H-Ras Expression Induces Fatty Acid Profile Changes in Human Fibroblasts and Extracellular Vesicles." International Journal of Molecular Sciences 19, no. 11 (2018): 3515. http://dx.doi.org/10.3390/ijms19113515.

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Extracellular vesicles (EVs) are lipid bilayer surrounded particles that are considered an additional way to transmit signals outside the cell. Lipids have not only a structural role in the organization of EVs membrane bilayer, but they also represent a source of lipid mediators that may act on target cells. Senescent cells are characterized by a permanent arrest of cell proliferation, but they are still metabolically active and influence nearby tissue secreting specific signaling mediators, including those carried by EVs. Notably, cellular senescence is associated with increased EVs release.
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Buchanan, F. G., M. McReynolds, A. Couvillon, et al. "Requirement of phospholipase D1 activity in H-RasV12-induced transformation." Proceedings of the National Academy of Sciences 102, no. 5 (2005): 1638–42. http://dx.doi.org/10.1073/pnas.0406698102.

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4

Sashida, Goro, Yan Liu, Shannon Elf, et al. "ELF4/MEF Activates MDM2 Expression and Blocks Oncogene-Induced p16 Activation To Promote Transformation." Molecular and Cellular Biology 29, no. 13 (2009): 3687–99. http://dx.doi.org/10.1128/mcb.01551-08.

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ABSTRACT Several ETS transcription factors, including ELF4/MEF, can function as oncogenes in murine cancer models and are overexpressed in human cancer. We found that Elf4/Mef activates Mdm2 expression; thus, lack of or knockdown of Elf4/Mef reduces Mdm2 levels in mouse embryonic fibroblasts (mef's), leading to enhanced p53 protein accumulation and p53-dependent senescence. Even though p53 is absent in Elf4−/− p53−/− mef's, neither oncogenic H-RasV12 nor c-myc can induce transformation of these cells. This appears to relate to the INK4a/ARF locus; both p19ARF and p16 are increased in Elf4−/− p
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Yoh, Kathryn E., Kausik Regunath, Asja Guzman, et al. "Repression of p63 and induction of EMT by mutant Ras in mammary epithelial cells." Proceedings of the National Academy of Sciences 113, no. 41 (2016): E6107—E6116. http://dx.doi.org/10.1073/pnas.1613417113.

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The p53-related transcription factor p63 is required for maintenance of epithelial cell differentiation. We found that activated forms of the Harvey Rat Sarcoma Virus GTPase (H-RAS) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) oncogenes strongly repress expression of ∆Np63α, the predominant p63 isoform in basal mammary epithelial cells. This regulation occurs at the transcriptional level, and a short region of the ∆Np63 promoter is sufficient for repression induced by H-RasV12. The suppression of ∆Np63α expression by these oncogenes concomitantly leads to
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6

Kang, Hyeji, Taerim Oh, Young Yil Bahk, et al. "HSF1 Regulates Mevalonate and Cholesterol Biosynthesis Pathways." Cancers 11, no. 9 (2019): 1363. http://dx.doi.org/10.3390/cancers11091363.

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Heat shock factor 1 (HSF1) is an essential transcription factor in cellular adaptation to various stresses such as heat, proteotoxic stress, metabolic stress, reactive oxygen species, and heavy metals. HSF1 promotes cancer development and progression, and increased HSF1 levels are frequently observed in multiple types of cancers. Increased activity in the mevalonate and cholesterol biosynthesis pathways, which are very important for cancer growth and progression, is observed in various cancers. However, the functional role of HSF1 in the mevalonate and cholesterol biosynthesis pathways has not
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7

Shuman, Jon D., Thomas Sebastian, Philipp Kaldis та ін. "Cell Cycle-Dependent Phosphorylation of C/EBPβ Mediates Oncogenic Cooperativity between C/EBPβ and H-RasV12". Molecular and Cellular Biology 24, № 17 (2004): 7380–91. http://dx.doi.org/10.1128/mcb.24.17.7380-7391.2004.

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ABSTRACT CCAAT/enhancer binding protein β (C/EBPβ) is a widely expressed transcription factor whose activity is regulated by oncogenic Ha-RasV12 signaling. C/EBPβ is essential for the development of mouse skin tumors containing Ras mutations and can cooperate with RasV12 to transform NIH 3T3 cells. Here we have investigated Ras-induced phosphorylation of C/EBPβ in fibroblasts and report a novel proline-directed phosphoacceptor site at Ser64 within the transactivation domain. Ser64 phosphorylation was induced by activated Ras and Raf but was not blocked by chemical inhibitors of MEK1/2, phospha
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8

Park, Kun-Young, Eun-Ju Cho, Sook-Hee Rhee, Keun-Ok Jung, Sun-Ju Yi та Byung H. Jhun. "Kimchi and an Active Component, β-Sitosterol, Reduce Oncogenic H-Rasv12-Induced DNA Synthesis". Journal of Medicinal Food 6, № 3 (2003): 151–56. http://dx.doi.org/10.1089/10966200360716544.

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9

De Alvaro, Cristina, Iria Nieto-Vazquez, Jose Maria Rojas та Margarita Lorenzo. "Nuclear Exclusion of Forkhead Box O and Elk1 and Activation of Nuclear Factor-κB Are Required for C2C12-RasV12C40 Myoblast Differentiation". Endocrinology 149, № 2 (2007): 793–801. http://dx.doi.org/10.1210/en.2007-0657.

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Activating ras point mutations are frequently found in skeletal muscle tumors such as rhabdomyosarcomas. In this study we investigated the impact of two different H-ras mutants in skeletal muscle differentiation: RasV12, a constitutively active form, and RasV12C40, a mutant deficient in Raf1 activation. Stably transfected C2C12-RasV12 myoblasts actively proliferated as indicated by the sustained expression of proliferating cell nuclear antigen and retinoblastoma at the hyperphosphorylated state and failed to express differentiation markers. This differentiation-defective phenotype was a conseq
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10

Teramoto, Hidemi, Maria Domenica Castellone, Renae L. Malek, et al. "Autocrine activation of an osteopontin-CD44-Rac pathway enhances invasion and transformation by H-RasV12." Oncogene 24, no. 3 (2004): 489–501. http://dx.doi.org/10.1038/sj.onc.1208209.

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Dissertations / Theses on the topic "H-RasV12"

1

Silva, Juliana Galvão da. "Efeito dual de FGF2 e PMA em células HEK 293 transformadas por H-rasV12." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-20012015-085930/.

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Sabe-se há décadas que mutações nos genes ras estão presentes em cerca de 20% dos cânceres humanos, mas o desenvolvimento de terapias eficazes para o tratamento de câncer dependente dos oncogenes ras permanece um desafio científico importante. Nesse contexto, o nosso grupo publicou recentemente resultados interessantes mostrando que FGF2 exógeno ou PMA, contrariamente à expectativa geral, inibem a proliferação de células de camundongo malignas dependentes dos oncogenes H- ou K-Ras. Para dar continuidade a estes estudos o projeto desta tese foi planejado para investigar os mecanismos subjacente
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2

Augereau, Adeline. "Nouveaux liens entre dysfonctionnement télomérique et cancer : cas de la Leucémie Lymphoïde Chronique et rôle de RasV12 dans la protection des télomères par TRF2." Thesis, Lyon, École normale supérieure, 2012. http://www.theses.fr/2012ENSL0753.

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Les télomères sont les extrémités des chromosomes et sont protégés par le complexe shelterin pour ne pas être reconnus comme des cassures accidentelles d'ADN double brin. Un enjeu majeur dans la recherche sur les télomères est de comprendre comment l'intégrité des extrémités des chromosomes au cours de l'oncogenèse est modifiée. La perte de répétitions télomériques à chaque division cellulaire peut être compensée par l’activité de l’enzyme télomérase qui ajoute "de novo" des motifs télomériques. Bien que la télomérase soit surexprimée dans la majorité des cellules cancéreuses, l’impact de modi
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